Teeth are subject to various diseases and problems, among which are caries, plaque, tartar, gingivitis, abusive whitening practices from use of concentrated hydrogen peroxide, hypersensitivity, and enamel staining.
Most oral care diseases originate with the thin proteinaceous film deposited as pellicle onto tooth surfaces. This serves as a substrate for bacteria and mineral deposits which harden into plaque and eventually tartar. The bacterial colonies sheltered therein absorb and metabolize nutrients from substances that pass through the oral cavity, particularly sucrose, and produce carboxylic acids. These acids are not readily rinsed away by the oral fluids because the colonies are protected and held in close proximity to the tooth surfaces by the plaque film. The acids produced, then, are held against the dental surfaces, where they slowly demineralize and destroy the hydroxyapatite crystal structure, producing caries. The calculus and tartar deposits cause separation of the gingival tissue from the tooth, causing inflammation and creating “pockets” which also provide a more sheltered, difficult to clean area for the destructive process. The receding gingiva eventually expose the dentinal tubules, which results in hypersensitivity.
Other, more esthetic problems are halitosis and tooth staining. The former is assuaged by treatment with flavorants, mouth fresheners and anti-bacterial agents in the toothpaste or mouthwash formulation. Anti-bacterial agents, such as triclosan and cetylpyridinium chloride, also kill cariogenic bacteria, hence serve an anti-caries function as well.
Separately, cetylpyridinium chloride, along with tea, coffee, wine, cigarette smoke and other factors may contribute to tooth staining. The popular methods of removing the stains are use of a more abrasive toothpaste formulation and/or a “whitening agent”, commonly hydrogen peroxide. The concentration of the peroxide is steadily increasing in response to consumers' desire for more rapid and complete stain and discoloration removal. The problem associated with these treatments is that the more abrasive toothpaste also wears down the tooth enamel and the peroxide also oxidizes the amelogenin matrix that controls the orderly formation of the hydroxyapatite crystals in the natural remineralization process. The more aggressive peroxide treatments have been associated with development of tooth hypersensitivity.
Simple organic phosphate ester surfactants have been shown to provide numerous oral care benefits, as described, for example, in U.S. Pat. Nos. 9,034,308 and 9,040,025 and references cited therein. Such esters have been shown to be effective cleaning agents for the removal of dental surface residues and form protective films that inhibit the adherence of Streptococcus mutans to hydroxyapatite. Caries Res. 1991; 25:51-57. Phosphate ester surfactants improve the efficacy of the anti-bacterial agents, such as triclosan, by enhancing its deposition and retention onto the tooth. U.S. Pat. Nos. 5,605,676, and 6,110,445. Similarly, phosphate ester surfactants have been claimed as an essential ingredient in a formulation with the milder carbamoyl peroxide as a potential replacement for hydrogen peroxide in toothpaste and mouthwash formulations. U.S. Publication No. 2009/0169493. The integrity of the phosphate ester surfactant films on hydroxyapatite was demonstrated by their ability to protect it from erosion by citric acid (fruit juices) and phosphoric acid (cola soft drinks). U.S. Publication Nos. 2008/0247973 and 2010/0316579.
JP 2007/284609 describes copolymers based solely on phosphate ester functional (meth)acrylic ester monomers, Monomer A (e.g. the phosphate ester of 2-hydroxyethyl methacrylate), the comonomers being selected from a wide variety of non-phosphate functional monomers, “B”, “C” and “D”, as being useful for stain prevention and inhibition of bacterial or proteinaceous film deposition onto the tooth surface.
Although the overall effectiveness of the phosphate ester surfactants to minimize or eliminate the above problems is good, the duration of the protection is limited by the structure. Both the monoalkyl and dialkyl phosphate esters have only a single phosphate ester moiety to serve as the point of attachment to the dental surface. The oral phosphatase enzymes can penetrate the surfactant film to eventually hydrolyze the phosphate ester link and destroy the film over a period estimated to be about six to eight hours. To be more in line with personal oral hygiene practices of once daily tooth brushing, it would be desirable to at least double this period of effectiveness and further improve the film integrity, durability and resistance to penetration.